Homocysteinemia is known to be one of risk factors of the development of myocardial infarction and arteriosclerosis. Precise mechanisms involved in it, however, have not yet been clarified, though such different hypotheses are proposed that are based on oxidation stress of homocysteine, impaired functioning of nitrogen oxide (NO), the endoplasmic reticulum put under stress, etc. Among these is the homocysteinethiolactone (hereinafter referred to as “HTL”) based hypothesis.